Fig. 17.31 ). In contrast to the left ventricle, reversal of blood flow does not occur in the right ventricle in early systole because pressure in the thin right ventricle is lower during systole. Hence, systolic blood flow constitutes a much greater proportion of total coronary inflow than it does in the left coronary artery.
•Fig. 17.32 A, Unmaskingoftherestrictingeffectofventricularsystoleonmeancoronarybloodflowbyinductionofventricularfibrillationduringperfusionoftheleftcoronaryarteryatconstantpressure.Withtheonsetofventricularfibrillation,coronarybloodflowincreasesabruptlybecauseextravascularcompressionisremoved.Flowthengraduallyreturnstowardandoftenfallsbelowtheprefibrillationlevel.Thisincreaseincoronaryresistancethatoccursdespitetheremovalofextravascularcompressiondemonstratestheheart’sabilitytoadjustitsbloodflowtomeetitsenergyrequirements.B, EffectofcardiacsympatheticnervestimulationoncoronarybloodflowandonbloodO2tension(PO2)inthecoronarysinusinafibrillatingheartduringperfusionoftheleftcoronaryarteryatconstantpressure.(BerneRM.Unpublishedobservations.)
The extent to which extravascular compression restricts coronary inflow can be readily observed when the heart is suddenly arrested in diastole or with the induction of ventricular fibrillation.
Fig. 17.32A depicts mean left coronary flow when the vessel was perfused with blood at a constant pressure from a reservoir. When ventricular fibrillation was electrically induced, blood flow increased immediately and substantially. A subsequent increase in coronary resistance over a period of many minutes reduced myocardial blood flow to below the level that existed before induction of ventricular fibrillation (see
Fig. 17.32B , just before stellate ganglion stimulation).
When diastolic pressure in the coronary arteries is abnormally low (as in severe hypotension, partial coronary artery occlusion, or severe aortic stenosis), the ratio of endocardial to epicardial blood flow falls below a value of 1. This ratio indicates that blood flow to the endocardial regions is more severely impaired than that to the epicardial regions of the ventricle. There is also an increase in the gradient of myocardial lactic acid and myocardial adenosine concentrations from epicardium to endocardium. For this reason, the myocardial damage observed in atherosclerotic heart disease (e.g., after coronary occlusion) is greatest in the inner wall of the left ventricle.
Tachycardia and bradycardia have dual effects on coronary blood flow. A change in heart rate mainly alters diastole. In tachycardia, the proportion of time spent in systole, and consequently the period of restricted inflow, increases. However, this mechanical effect is overridden by the dilation of coronary resistance vessels associated with the increased metabolic activity of the more rapidly beating heart. With bradycardia, the opposite occurs: Coronary inflow is less restricted (more time spent in diastole), but so are the metabolic (O2) requirements of the myocardium.
Stimulation of cardiac sympathetic nerves markedly increases coronary blood flow. However, the increase in flow is associated with an increased heart rate and more forceful systole. The stronger contraction and the tachycardia tend to restrict coronary flow. The increase in myocardial metabolic activity, however, tends to dilate coronary resistance vessels. The increase in coronary blood flow evoked by cardiac sympathetic nerve stimulation reflects the sum of these factors. In perfused hearts in which the mechanical effect of extravascular compression is eliminated by cardiac arrest or by ventricular fibrillation, an initial coronary vasoconstriction of the coronary vessels is often observed. After this initial vasoconstriction, the metabolic effect evokes vasodilation (see
Fig. 17.32B